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L McIntosh

Publications and source records attributed to L McIntosh.

At least 19 recordsLinked to original sources
PubMed2004

Mitochondria/nuclear signaling of alternative oxidase gene expression occurs through distinct pathways involving organic acids and reactive oxygen species.

Cultured cells of tobacco (Nicotiana tabacum L. cv Petit Havana) were used to investigate signals regulating the expression of the "model" nuclear gene encoding the alternative oxidase (AOX) (AOX1), the terminal oxidase of the mitochondrial alternative respiratory pathway. Several conditions shown to induce AOX1 mRNA accumulation also result in an increase in cellular citrate concentrations, suggesting that citrate and/or other tricarboxylic acid (TCA) cycle intermediates may be important signal metabolites. In addition, mitochondrial reactive oxygen species (ROS) production has recently been shown to be a factor mediating mitochondria-to-nucleus signaling for the expression of AOX1. We found that the exogenously supplied TCA cycle organic acids citrate, malate and 2-oxoglutarate caused rapid and dramatic increases in the steady-state level of AOX1 mRNA at low, near physiological concentrations (0.1 mM). Furthermore, an increase in AOX1 induced by the addition of organic acids occurs independently of mitochondrial ROS formation. Our results demonstrate that two separate pathways for mitochondria-to-nucleus signaling of AOX1 may exist, one involving ROS and the other organic acids.

Cell Nucleus↗
PubMed2004

A phase I study of AMD473 and docetaxel given once every 3 weeks in patients with advanced refractory cancer: a National Cancer Institute of Canada-Clinical Trials Group trial, IND 131.

BACKGROUND: AMD473 (previously ZD0473) is a new-generation platinum compound with activity against a wide range of human tumour cell lines and xenografts, including carboplatin- and cisplatin-resistant lines. To assess its potential combined with a taxane, a phase I study of AMD473 and docetaxel in advanced cancer was initiated by the National Cancer Institute of Canada-Clinical Trials Group. PATIENTS AND METHODS: Patients with advanced cancer, measurable disease, performance status Eastern Cooperative Oncology Group 0-2, no major organ dysfunction, and one or no previous taxane regimen received escalating doses of AMD473 and docetaxel every 3 weeks, with a starting dose of AMD473 80 mg/m(2) and docetaxel 60 mg/m(2). RESULTS: Thirty-three patients enrolled on four dose levels were evaluable for toxicity and 25 patients were evaluable for response. The maximum tolerated dose was dose level 4 (AMD473 120 mg/m(2) and docetaxel 75 mg/m(2)), with grade 4 neutropenia in both minimally and heavily pretreated patients causing dose-limiting toxicity. As well at dose level 4, one patient had grade 3 vomiting despite premedication. Dose level three was expanded for both groups of patients and was defined as the recommended phase II dose at AMD473 100 mg/m(2) and docetaxel 75 mg/m(2). Non-hematologic toxicities included fatigue, diarrhoea and other mild toxicities. There was one partial response in a patient with prostate cancer and stable disease in 15 patients. No apparent pharmacokinetic interaction was noted. CONCLUSION: AMD473 and docetaxel can be combined with a recommended phase II dose level of 100 mg/m(2) and 75 mg/m(2), respectively, given intravenously every 3 weeks. The combination has activity and should be explored in responsive tumour types.

Adenocarcinoma↗
PubMed2003

Phase II study of troxacitabine (BCH-4556) in patients with advanced and/or metastatic renal cell carcinoma: a trial of the National Cancer Institute of Canada-Clinical Trials Group.

PURPOSE: A multi-institution phase II study was undertaken by National Cancer Institute of Canada-Clinical Trials Group to evaluate the efficacy and toxicity of intravenous troxacitabine (Troxatyl; Shire Pharmaceuticals Plc, Laval, Quebec, Canada), in patients with renal cell carcinoma. PATIENTS AND METHODS: Between June 1999 and March 2000, 35 patients (24 male) with a mean age of 60 years who had advanced and/or metastatic disease were treated with troxacitabine given as an intravenous infusion over 30 minutes at a dose of 10 mg/m2 intravenously, once every 3 weeks. RESULTS: Of the 33 of 35 patients evaluable for response, there were two confirmed partial responses, 21 patients had stable disease (median duration, 4.4 months), and 10 patients had progressive disease. Eight patients remained stable for more than 6 months, of whom six remain free of progression. The most common drug-related nonhematologic toxicities observed were skin rash (77.1%), hand-foot syndrome (68.6%), alopecia (51.4%), fatigue (51.4%), and nausea (57.1%). Out of a total of 145 cycles of treatment, 98 were given without steroid premedication, whereas 47 cycles were given with steroid premedication. Without premedication, skin rash occurred in 37% of cycles compared with 26% when steroids were given prophylactically. CONCLUSION: Troxacitabine given at a dose of 10 mg/m2 once every 3 weeks was well tolerated in patients with metastatic renal cell cancer, with common toxicities being a moderate to severe granulocytopenia and skin rash. Steroid premedication may reduce the frequency and severity of the skin rash. Our current study suggests that the nucleoside analog troxacitabine may have modest activity against renal cell carcinoma; however, larger studies are required to confirm this.

Aged↗
PubMed2003

Phase II study of CGP 69846A (ISIS 5132) in recurrent epithelial ovarian cancer: an NCIC clinical trials group study (NCIC IND.116).

OBJECTIVE: ISIS 5132 is a 20-base phosphorothioate DNA oligonucleotide against human c-raf kinase, a downstream effector of ras oncogene function. C-raf kinase is a molecule in the MAP kinase signaling cascade which is essential for cellular proliferation, the overexpression of which leads to malignant expression. Activity of this compound was documented in a woman with ovarian cancer in a Phase I study. METHODS: We evaluated ISIS 5132 at a dose of 4 mg/kg/day by continuous venous infusion, administered for 21 days q 4 weeks in 22 patients with recurrent ovarian cancer in a standard two-stage Phase II design. Three patients were ineligible; 19 patients are evaluable for toxicity and 16 for response. All patients had previously received systemic therapy for ovarian cancer (6 had one and 13 had two prior regimens). Patients were treated with a median of two cycles and 79% of the patients received >90% planned dose intensity. RESULTS: ISIS 5132 was well tolerated with no episodes of Grade 3 or 4 hematologic or biochemical (creatinine, AST, bilirubin) toxicity. There were six episodes of grade 3 nonhematologic toxicity in 4 patients thought to be treatment related (lethargy 2; anorexia 1; abdominal pain 2; shortness of breath 1). No responses were seen in the 16 patients who are evaluable for response; 4 had stable disease for a median of 3.8 months and 12 patients had documented progressive disease. CONCLUSION: ISIS 5132 at 4 mg/kg/day as a single agent did not show activity in recurrent ovarian cancer.

Adult↗
PubMed2002

Vasorelaxant properties of isolated human radial arteries: comparison with internal mammary arteries.

Radial arteries, used in revascularisation surgery, are prone to spasm. We have examined the ability of nitrovasodilators, calcium channel blockers, and K(ATP) channel openers to cause vasodilation, and to attenuate contractions due to depolarisation and receptor activation in radial and mammary arteries used in coronary artery bypass graft surgery. Two to three millimetre rings of artery obtained from patients at surgery were studied in organ baths in vitro. Constriction to KC1 and phenylephrine was examined before and again after treatment of the rings with drug or vehicle. Calcium channel blockers were the only compounds to inhibit contractions to both KC1 and phenylephrine. Sodium nitroprusside attenuated constriction to phenylephrine but not KC1 in both vessels. K(ATP) channel openers similarly attenuated constriction to phenylephrine in radial arteries but were much less effective in mammary arteries. These studies support the continued use of calcium blockers after revascularisation with radial artery but suggest that other classes of drug may be as effective at minimising spasm due to receptor mediated constriction.

Adult↗
PubMed2001

Interactions among ascorbate, dehydroascorbate and glucose transport in cultured hippocampal neurons and glia.

There is an increasing recognition of the damaging role played by oxygen radicals in mediating necrotic neuronal injury. As such, it becomes important to understand the transport mechanisms that help maintain appropriate levels of small molecule antioxidants such as ascorbate in the brain. It has long been known that the transport of dehydroascorbate (DHA) into a variety of cell types is accomplished through the Glut-1 glucose transporter. In this paper, we characterize interactions among the transports of ascorbate, DHA and glucose in hippocampal cultures. We find: (a) sodium-dependent transport of ascorbate in mixed neuronal/glial, pure glial, and neuron-enriched hippocampal cultures; in contrast, we observed no such transport of DHA; (b) such ascorbate transport appeared to be independent of the glucose transporter, in that glucose did not compete for such transport, and overexpression of the Glut-1 glucose transporter did not alter ascorbate uptake; (c) in contrast, ascorbate, at concentrations ranging from 1 to 20 mM inhibited 2-dexogyglucose transport in mixed, glial and enriched neuronal hippocampal cultures; (d) potentially, ascorbate, by acting as an electron donor, could impair the function of molecules involve in the transport or metabolism of glucose. We observed mild inhibition of glucose transport by one unrelated electron donor (glutathione). Moreover, transport was also inhibited by an ascorbate analog which is not an electron donor. Thus, we conclude that ascorbate transport in hippocampal neurons and glia occurs independent of the glucose transporter but that, nevertheless, ascorbate, at concentrations generally thought to be supraphysiological, has the potential for disrupting glucose transport.

Animals↗
PubMed2001

Role of copper ions and cytochrome P450 in the vasodilator actions of the nitroxyl anion generator, Angeli's salt, on rat aorta.

Since copper ions catalyse the oxidation of nitroxyl anion to nitric oxide, we investigated whether this might explain the vasodilator actions of the nitroxyl generator, Angeli's salt, in rat aorta. Parallel studies were conducted with S-nitroso-N-acetyl-D,L-penicillamine (SNAP), since Cu ions catalyse the liberation of nitric oxide from this compound. Copper sulphate enhanced relaxation to Angeli's salt and SNAP but this resulted from reduced destruction of nitric oxide by superoxide rather than from enhanced generation of nitric oxide, since it was mimicked by superoxide dismutase and by the superoxide dismutase mimetic, MnCl2. Results with the selective Cu2+ chelators, neocuproine and bathocuproine disulfonate, and the Cu2+ chelators, EDTA, cuprizone and diethyldithiocarbamate, confirmed an important role for endogenous copper in mediating relaxation to SNAP but suggested only a minor role for Angeli's salt. Relaxation to Angeli's salt was, however, powerfully blocked by proadifen, suggesting an important role for cytochrome P450.

Animals↗
PubMed2001

Isolation of a CONSTANS ortholog from Pharbitis nil and its role in flowering.

The short-day plant Pharbitis nil is a model plant for the study of photoperiodic control of floral initiation. Flower formation can be induced at the cotyledon stage by a single long night of at least 14 h in duration. Using differential display of mRNA we identified a P. nil ortholog of the Arabidopsis CONSTANS (CO) gene, which will be referred to as PnCO. Expression of PnCO was high after a 14-h night, but low when the dark period was 12 h or less. Our results indicate that the level of the PnCO transcript is photoperiodically regulated. After transfer from continuous light to darkness, PnCO showed a circadian pattern of expression. Expression of the CAB gene, which is a molecular marker for the circadian clock, exhibited a different pattern of expression than did PnCO and was not subject to the same photoperiodic control. A major portion of the PnCO transcripts contained an unspliced intron. Only the intron-free PnCO was able to complement the co mutant of Arabidopsis by shortening the time to flower.

Amino Acid Sequence↗
PubMed1999

The alternative oxidase lowers mitochondrial reactive oxygen production in plant cells.

Besides the cytochrome c pathway, plant mitochondria have an alternative respiratory pathway that is comprised of a single homodimeric protein, alternative oxidase (AOX). Transgenic cultured tobacco cells with altered levels of AOX were used to test the hypothesis that the alternative pathway in plant mitochondria functions as a mechanism to decrease the formation of reactive oxygen species (ROS) produced during respiratory electron transport. Using the ROS-sensitive probe 2',7'-dichlorofluorescein diacetate, we found that antisense suppression of AOX resulted in cells with a significantly higher level of ROS compared with wild-type cells, whereas the overexpression of AOX resulted in cells with lower ROS abundance. Laser-scanning confocal microscopy showed that the difference in ROS abundance among wild-type and AOX transgenic cells was caused by changes in mitochondrial-specific ROS formation. Mitochondrial ROS production was exacerbated by the use of antimycin A, which inhibited normal cytochrome electron transport. In addition, cells overexpressing AOX were found to have consistently lower expression of genes encoding ROS-scavenging enzymes, including the superoxide dismutase genes SodA and SodB, as well as glutathione peroxidase. Also, the abundance of mRNAs encoding salicylic acid-binding catalase and a pathogenesis-related protein were significantly higher in cells deficient in AOX. These results are evidence that AOX plays a role in lowering mitochondrial ROS formation in plant cells.

Arabidopsis↗
PubMed1999

Physicians' perceptions of the effect on clinical services of an alternative funding plan at an academic health sciences centre.

BACKGROUND: In July 1994 an alternative funding plan for clinical services (global funding instead of fee-for-service payment) was established at the Southeastern Ontario Health Sciences Centre, Kingston, Ont. This study describes the perceptions of the referring physicians and consultants of the effects of the alternative funding plan 2.5 years after it was initiated. METHODS: A questionnaire was mailed to all physicians in the Kingston area in November 1996. Information was collected on demographics, referring physicians' perceptions of the funding plan's impact on their practices, consultants' perceptions of its impact on their activities, perceptions of referring and consultant physicians of its impact on services provided by consultants, and attitudes toward alternative funding in the context of the Ontario health care system. RESULTS: Of the 772 physicians 531 (68.8%) returned a completed questionnaire (323 referring physicians and 208 consultants). A sizeable proportion of the referring physicians (126 [39.0%]) indicated that they were referring fewer patients to consultants at the study centre. They did not think that their practice volume had increased, but they did report spending more time on complex cases and on patient care after referral or hospital stay, and more time coordinating community care after hospital stay. Of the consultants 81 (38.9%) believed that their time spent on patient care had increased. No consistent impact on time spent on research or teaching activities was perceived. A total of 54 (26.0%) of the consultants were concerned about the impact of the alternative funding plan on quality of care. A significant proportion of the respondents (399 [75.1%]) believed that outpatient waiting times had increased, and 116 (35.9%) of the referring physicians believed that consultants were not as available by telephone. Most (220 [68.1%]) of the referring physicians believed that the funding change had had a negative effect on health care services in the region, and 87 (41.8%) of the consultants agreed. Nevertheless, the respondents believed that other factors such as funding cuts, hospital bed closures and staff layoffs were much more responsible than the alternative funding plan for their negative perceptions. INTERPRETATION: The alternative funding plan appears to have had an impact on the practices of individual physicians. However, it was not the focus for significant opposition or support from either consultants participating in the funding plan or referring physicians.

Academic Medical Centers↗
PubMed1999

The cysteine-proximal aspartates in the Fx-binding niche of photosystem I. Effect of alanine and lysine replacements on photoautotrophic growth, electron transfer rates, single-turnover flash efficiency, and EPR spectral properties.

The FX electron acceptor in Photosystem I (PS I) is a highly electronegative (Em = -705 mV) interpolypeptide [4Fe-4S] cluster ligated by cysteines 556 and 565 on PsaB and cysteines 574 and 583 on PsaA in Synechocystis sp. PCC 6803. An aspartic acid is adjacent to each of these cysteines on PsaB and adjacent to the proline-proximal cysteine on PsaA. We investigated the effect of D566PsaB and D557PsaB on electron transfer through FX by changing each aspartate to the neutral alanine or to the positively charged lysine either singly (D566APsaB, D557APsaB, D566KPsaB, and D557KPsaB) or in pairs (D557APsaB/D566APsaB and D557KPsaB/D566APsaB). All mutants except for D557KPsaB/D566APsaB grew photoautotrophically, but the growth of D557KPsaB and D557APsaB/D566APsaB was impaired under low light. The doubling time was increased, and the chlorophyll content per cell was lower in D557KPsaB and D557APsaB/D566APsaB relative to the wild type and the other mutants. Nevertheless, the rates of NADP+ photoreduction in PS I complexes from all mutants were no less than 75% of that of the wild type. The kinetics of back-reaction of the electron acceptors on a single-turnover flash showed efficient electron transfer to the terminal acceptors FA and FB in PS I complexes from all mutants. The EPR spectrum of FX was identical to that in the wild type in all but the single and double D566APsaB mutants, where the high-field resonance was shifted downfield. We conclude that the impaired growth of some of the mutants is related to a reduced accumulation of PS I rather than to photosynthetic efficiency. The chemical nature and the charge of the amino acids adjacent to the cysteine ligands on PsaB do not appear to be significant factors in the efficiency of electron transfer through FX.

Alanine↗
PubMed1998

Dystrophy and myogenesis in mdx diaphragm muscle.

In order to determine why the diaphragm is more severely affected by progressive dystrophy than limb muscles in the mdx mouse, we examined how regional variations in diaphragm dystrophy, the measures of disease and repair, proliferation by committed myogenic cells, and the expression of mitogenic basic fibroblast growth factor (bFGF) could contribute to muscle-specific disease phenotypes. There were regional variations in new myotube formation in the diaphragm, with disease more severe in crural than costal leaflets. New repair increased in hyperthyroidism without changes in accumulated repair, probably due to fiber loss. General proliferation was nearly twofold higher in limb than diaphragm mononuclear cells. Since only 2.5-8.4% of committed muscle precursors were proliferating, the higher proliferation by myf5+ myogenic cells in diaphragm did not account for muscle-specific differences. Proliferation by bFGF+ mononuclear cells and an immunogold labeling index for bFGF protein in diaphragm myoblasts were lower in diaphragm than limb muscle. In culture, mixed limb myoblast and fibroblasts contained more S phase cells than diaphragm cells, although myoblasts cycled similarly between muscles. Therefore while muscle architecture and the formation and number of new myotubes certainly affect disease phenotype, the differential outcome of regeneration in mdx diaphragm and limb muscle appears to be contributed by both nonmyogenic and myogenic cells.

Animals↗
PubMed1998

Nuclear magnetic resonance spectroscopy study of muscle growth, mdx dystrophy and glucocorticoid treatments: correlation with repair.

Proton nuclear magnetic resonance spectroscopy (1H NMR) can be used to study skeletal muscle metabolism. The mdx mouse is a unique animal for studies of muscle regeneration, and models the disease of Duchenne muscular dystrophy (DMD). The goals of this study were to determine the potential of 1H NMR spectroscopy as an alternative to conventional histology in monitoring: (1) normal growth in control muscle and the progression of dystrophy in mdx muscle, and (2) beneficial treatments (glucocorticoids) on mdx dystrophy. Ex vivo 1H NMR spectra of limb and diaphragm muscles were obtained from different ages of control and mdx mice, and from mice which were treated with prednisone or deflazacort. Peaks with contributions from creatine, taurine and lipids were examined. Lower levels of taurine and creatine characterized predystrophy and active dystrophy intervals in mdx muscle compared to control. Levels of taurine increased with stabilization of the disease by repair. A measure of accumulated muscle repair, fiber centronucleation and many spectral peaks were highly and significantly correlated. Greater amounts of lipids were found in the diaphragm compared to limb spectra. Treatment of dystrophy, which improved muscle phenotype, resulted in greater levels of taurine and creatine, especially in the limb muscle. Therefore, 1H NMR differentially discriminates: (1) control and mdx muscle; (2) the progression of mdx dystrophy and developmental stages in normal growth; (3) mild and severe dystrophic phenotypes (diaphragm vs limb); and (4) changes associated with improved muscle phenotype and regeneration (due to treatment or injury). The results focus on monitoring muscle repair, not degeneration. We conclude that 1H NMR is a reliable tool in the objective investigation of muscle repair status during muscular dystrophy.

Animals↗
PubMed1998

Molecular localization of a redox-modulated process regulating plant mitochondrial electron transport

Using in organellar assays, we found that significant tobacco alternative oxidase (AOX) activity is dependent on both reduction of a putative regulatory disulfide bond and the presence of pyruvate, which may interact with a Cys sulfhydryl. This redox modulation and pyruvate activation thus may be important in determining the partitioning of electrons to AOX in vivo. To investigate these regulatory mechanisms, we generated tobacco plants expressing mutated AOX proteins. Mutation of the most N-terminal Cys residue (Cys-126) to an Ala residue produced an AOX that could not be converted to the disulfide-linked form, thus identifying this Cys residue as being responsible for redox modulation. Although this mutation might be expected to produce an AOX with constitutive high activity in the presence of pyruvate, we found it to have minimal in organellar activity in the presence of pyruvate. Nonetheless, the Cys-126 mutation did not appear to have compromised the catalytic function of AOX, given that cells expressing the protein displayed high rates of cyanide-resistant respiration in vivo. The striking difference between in vivo and in organellar results suggests that an additional mechanism(s), as yet unidentified by in organellar assays, may promote activity in vivo. Mutation of the Cys residue nearest the presumptive active site (Cys-176) to an Ala residue did not prevent disulfide bond formation or affect the ability of AOX to be stimulated by pyruvate, indicating that this Cys residue is involved in neither redox modulation nor pyruvate activation.

Journal Article↗
PubMed1997

Strains of synechocystis sp. PCC 6803 with altered PsaC. I. Mutations incorporated in the cysteine ligands of the two [4Fe-4S] clusters FA and FB of photosystem I.

Two [4Fe-4S] clusters, FA and FB, function as terminal electron carriers in Photosystem I (PS I), a thylakoid membrane-bound protein-pigment complex. To probe the function of these two clusters in photosynthetic electron transport, site-directed mutants were created in the transformable cyanobacterium Synechocystis sp. PCC 6803. Cysteine ligands in positions 14 or 51 to FB and FA, respectively, were replaced with aspartate, serine, or alanine, and the effect on the genetic, physiological, and biochemical characteristics of PS I complexes from the mutant strains were studied. All mutant strains were unable to grow photoautotrophically, and compared with wild type, mixotrophic growth was inhibited under normal light intensity. The mutant cells supported lower rates of whole-chain photosynthetic electron transport. Thylakoids isolated from the aspartate and serine mutants have lower levels of PS I subunits PsaC, PsaD, and PsaE and lower rates of PS I-mediated substrate photoreduction compared with the wild type. The alanine and double aspartate mutants have no detectable levels PsaC, PsaD, and PsaE. Electron transfer rates, measured by cytochrome c6-mediated NADP+ photoreduction, were lower in purified PS I complexes from the aspartate and serine mutants. By measuring the P700(+) kinetics after a single turnover flash, a large percentage of the backreaction in the aspartate and serine mutants was found to be derived from A1 and FX, indicating an inefficiency at the FX --> FA/FB electron transfer step. The alanine and double aspartate mutants failed to show any backreaction from [FA/FB]-. These results indicate that the various mutations of the cysteine 14 and 51 ligands to FB and FA affect biogenesis and electron transfer differently depending on the type of substitution, and that the effects of mutations on biogenesis and function can be biochemically separated and analyzed.

Cyanobacteria↗
PubMed1997

Strains of Synechocystis sp. PCC 6803 with altered PsaC. II. EPR and optical spectroscopic properties of FA and FB in aspartate, serine, and alanine replacements of cysteines 14 and 51.

A psaC deletion mutant of the unicellular cyanobacterium Synechocystis sp. PCC 6803 was utilized to incorporate site-specific amino acid substitutions in the cysteine residues that ligate the FA and FB iron-sulfur clusters in Photosystem I (PS I). Cysteines 14 and 51 of PsaC were changed to aspartic acid (C14DPsaC, C51DPsaC, C14D/C51DPsaC), serine (C14SPsaC, C51SPsaC), and alanine (C14APsaC, C51APsaC), and the properties of FA and FB were characterized by electron paramagnetic resonance spectroscopy and time-resolved optical spectroscopy. The C14DPsaC-PS I and C14SPsaC-PS I complexes showed high levels of photoreduction of FA with g values of 2.045, 1. 944, and 1.852 after illumination at 15 K, but there was no evidence of reduced FB in the g = 2 region. The C51DPsaC-PS I and C51SPsaC-PS I complexes showed low levels of photoreduction of FB with g values of 2.067, 1.931, and 1.881 after illumination at 15 K, but there was no evidence of reduced FA in the g = 2 region. The presence of FB was inferred in C14DPsaC-PS I and C14SPsaC-PS I, and the presence of FA was inferred in C51DPsaC-PS I and C51SPsaC-PS I by magnetic interaction in the photoaccumulated spectra and by the equal spin concentration of the irreversible P700(+) cation generated by illumination at 77 K. Flash-induced optical absorbance changes at 298 K in the presence of a fast electron donor indicate that two electron acceptors function after FX in the four mutant PS I complexes at room temperature. These data suggest that a mixed-ligand [4Fe-4S] cluster is present in the mutant sites of C14X-PS I and C51X-PS I (where X = D or S), but that the proposed spin state of S = 3/2 renders the resonances undetectable in the g = 2 region. The C14APsaC-PS I, C51APsaC-PS I and C14D/C51DPsaC-PS I complexes show only the photoreduction of FX, consistent with the absence of PsaC. These results show that only those PsaC proteins that contain two [4Fe-4S] clusters are capable of assembling onto PS I cores in vivo.

Amino Acids↗